Renal damage occurs acutely in response to metals and certain drugs, and chronically in response to a variety of insults. In both cases, renal damage is presently diagnosed when it is extensive enough to cause alterations of renal excretory and blood pressure regulating functions which give rise to clinically detectable signs and symptoms (e.g. serum creatinine increment, increased proteinuria, etc.). For these clinical parameters to show up, it is necessary that at least the equivalent to the function of 2/3 of the total number of nephrons be nullified. At such a point of diagnosis, damage is very extensive and thus treatment very difficult. Accordingly, a priority therapeutic need is the identification of novel markers of "hidden" damage, present in readily available biological samples (e.g. urine), which allow a subtler determination of renal damage. With this objective, we have used a known rat model of acute renal damage induced by the aminoglycoside antibiotic gentamicin to collect urine samples from control and nephrotoxic animals from which to investigate the presence of new types of markers associated to the administration of gentamicin and to renal deterioration. New markers identified, which are related to renal pathophysiological events, may open up new sources of potential markers of hidden (subclinical) damage with applicability in both acute and chronic renal disease. By western blot and ELISA, we have been able to identify presence of collagen I, procollagen I carboxyterminal peptide and bone morphogenic protein 7 in the urine from nephrotoxic animals but not in that of controls.